| First Author | Mizgerd JP | Year | 2002 |
| Journal | Physiol Genomics | Volume | 12 |
| Issue | 1 | Pages | 47-51 |
| PubMed ID | 12407184 | Mgi Jnum | J:82610 |
| Mgi Id | MGI:2653799 | Doi | 10.1152/physiolgenomics.00073.2002 |
| Citation | Mizgerd JP, et al. (2002) Exon truncation by alternative splicing of murine ICAM-1. Physiol Genomics 12(1):47-51 |
| abstractText | The murine gene for intercellular adhesion molecule-1 (ICAM-1) encodes multiple products, arising from alternative splicing. Full-length ICAM-1 contains five extracellular Ig domains, each encoded by a separate exon. Alternatively spliced forms have Ig domains 2, 3, and/or 4 excised as a result of exon skipping. We report here a novel splice variant of murine ICAM-1, resulting from exon truncation rather than exon skipping and affecting Ig domain 5. A 5' splice donor site within exon 6 generates transcripts missing 69 nucleic acids from the 3' terminus of the exon. This in-frame exon truncation is predicted to replace 24 amino acids within Ig domain 5 with a single aspartic acid residue, yielding a structure other than an Ig domain immediately external to the membrane. Expression of this alternatively spliced form is induced in mouse lungs, spleen, and kidneys during LPS-induced pulmonary inflammation. Since the affected region is critical for ICAM-1 presentation, dimerization, and solubilization, this alternative splice variant may have unique physiological functions. |
